Since the concept of defective DSB repair by the LOF of BRCA1 protein aids in chemotherapy of BRCA1/2 deficient cancers by hyper-sensitizing cells to Poly (ADP-ribose) polymerase (PARP) inhibitors, a study [64] set out to understand the mechanisms by which resistant clones of PARP inhibitors arise, specifically focusing on the loss of 53BP1-encoded by the TP53BP1 gene and its associated co-factors. The gene discussed is TP53BP1; the disease is cancer.